ANALYSIS OF CELLULAR FACTORS AFFECTING RETROVIRUS INFECTION AND GROWTH

本项目的重点是细胞限制的机制。 逆转录病毒在猫细胞中的生长。此前曾有数据显示， 猫内源性病毒RD114在侵入后受到限制 而不是在前病毒整合和表达的水平上。 最近的结果表明，这种限制是基于限制性的 细胞不能完全处理主要的包膜糖蛋白 RD114病毒和RD114颗粒的同时不能 含有未经处理的环境病毒产品，以引发非 允许的单元格。这代表了一种新的病毒限制机制。 然而，结果也表明，某些细胞可以被这种 病毒和完整的环境处理并不是绝对要求 因为病毒的传染性。 限制嗜淋巴猫慢病毒在贴壁细胞中的表达 一系列涉及克隆的嵌合病毒结构的分析 在贴壁细胞中复制的FIV Petaluma毒株，以及 对嗜淋巴的PPR菌株也进行了研究。结果 表明涉及病毒包膜基因的阻断，最有可能 涉及细胞受体，阻止PPR在粘附物中传播的能力 细胞。然而，有证据也表明，PPR的表达受到抑制 在穿透后水平的非贴壁细胞中，意味着第二个阻塞 到限制性细胞中的感染。

This project has focused on the mechanisms of cellular restriction of retroviral growth in feline cells. It was previously shown that the feline endogenous virus, RD114, was restricted at a post-penetration level, rather than at the level of provirus integration and expression. Recent results show that this restriction is based on the restrictive cells' inability to completely process the major envelope glycoprotein of the RD114 virus, and the concurrent inability of RD114 particles containing unprocessed env products to initiate infection of non- permissive cells. This represents a novel mechanism of virus restriction. Results also suggest, however, that certain cells can be infected by such viruses and that complete env processing is not an absolute requirement for viral infectivity. Restriction of lymphotropic feline lentiviruses in adherent cells through the analysis of a series of chimeric virus constructs involving clones of the Petaluma strain of FIV, which replicates in adherent cells, and the PPR strain, which is lymphotropic, have also been investigated. Results indicate that a block involving the viral env gene, most probably involving a cell receptor, blocks PPR's ability to spread in adherent cells. However, evidence also suggests that PPR expression is suppressed in non-adherent cells at a post-penetration level, implying a second block to infection in restrictive cells.